针刺联合优质护理干预对周围性面神经麻痹急性期患者的影响

目的分析针刺联合优质护理干预对周围性面神经麻痹急性期患者的影响。方法以2016年1月—2019年2月60例周围性面神经麻痹急性期患者为研究对象,患者按照护理方法不同,将其分为对照组、观察组各30例患者,对照组进行神经内科的常规护理,观察组进行针刺联合优质护理干预,对2组患者临床疗效和护理满意度等进行观察。结果对照组总有效率为70%,观察组总有效率为96.6%(P<0.05)。对照组护理满意度为63.3%,观察组护理满意度为96.6%(P<0.05)。结论周围性面神经麻痹急性期患者临床治疗中,针刺联合优质护理干预的应用,可以提升患者临床疗效,降低患者住院时间,实现其护理满意度的提升。     

水针疗法联合清热祛毒汤治疗寻常型银屑病(血热证)的疗效及其作用机制分析

目的观察分析水针疗法联合清热祛毒汤治疗寻常型银屑病(血热证)的疗效及其作用机制。方法选择2018年8月—2019年7月在我院接收治疗的112例寻常型银屑病患者作为分析对象,采取随机分组的办法将其分为对照组56例和研究组56例,对照组患者采取水针疗法治疗,研究组在对照组的基础上联合清热祛毒汤治疗。比较分析2组患者的疗效;治疗前后的中医证候评分、皮肤病生活质量指数(DLQI)评分;治疗前后皮损面积、浸润、鳞屑、红斑等评分;治疗前后肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、血管内皮生长因子(VEGF)水平变化情况。结果研究组患者治疗总有效率89.29%明显高于对照组73.21%(P<0.05);治疗前,2组患者的中医证候评分、DLQI评分、皮损面积、浸润、鳞屑、红斑等评分及TNF-α、IL-6、VEGF等水平比较(P>0.05);研究组患者治疗后的中医证候评分与DLQI评分明显低于治疗前(P<0.05);研究组患者治疗后的皮损面积、浸润、鳞屑、红斑等评分明显低于对照组(P<0.05);研究组患者治疗后的TNF-α、IL-6、VEGF等水平明显低于对照组(P<0.05)。结论对寻常型银屑病患者采取水针疗法联合清热祛毒汤治疗的疗效显著,能有效改善中医证候表现,提高生活质量,减轻皮损程度,降低炎症反应,其作用机制可能与炎症因子水平、皮损血管增生相关。     

气血同治法治疗胃息肉验案1则

胃息肉在消化道息肉中最常见,疾病早期多无明显症状,即使有临床症状也无特异性,主要表现为上腹疼痛和腹胀等症,极易造成漏治和误治,在很大程度上影响患者的生活质量。于春泉主任总结多年临床经验,在治疗胃息肉方面有独到的见解,以气血同治为治疗法则,通过补气、行气、活血和养血等治法扶正祛邪,恢复脏腑气血阴阳动态平衡,标本兼顾,临床效果可观。     

INAUGURAL ARTICLE by a Recently Elected Academy Member:Functional redundancy of type I and type II receptors in the regulation of skeletal muscle growth by myostatin and activin A

Myostatin (MSTN) is a transforming growth factor-β (TGF-β) family member that normally acts to limit muscle growth. The function of MSTN is partially redundant with that of another TGF-β family member, activin A. MSTN and activin A are capable of signaling through a complex of type II and type I receptors. Here, we investigated the roles of two type II receptors (ACVR2 and ACVR2B) and two type I receptors (ALK4 and ALK5) in the regulation of muscle mass by these ligands by genetically targeting these receptors either alone or in combination specifically in myofibers in mice. We show that targeting signaling in myofibers is sufficient to cause significant increases in muscle mass, showing that myofibers are the direct target for signaling by these ligands in the regulation of muscle growth. Moreover, we show that there is functional redundancy between the two type II receptors as well as between the two type I receptors and that all four type II/type I receptor combinations are utilized in vivo. Targeting signaling specifically in myofibers also led to reductions in overall body fat content and improved glucose metabolism in mice fed either regular chow or a high-fat diet, demonstrating that these metabolic effects are the result of enhanced muscling. We observed no effect, however, on either bone density or muscle regeneration in mice in which signaling was targeted in myofibers. The latter finding implies that MSTN likely signals to other cells, such as satellite cells, in addition to myofibers to regulate muscle homeostasis.

Myostatin (MSTN) is a secreted signaling molecule that normally acts to limit skeletal muscle growth (for review, see ref. 1). Mice lacking MSTN exhibit dramatic increases in muscle mass throughout the body, with individual muscles growing to about twice the normal size (2). MSTN appears to play two distinct roles in regulating muscle size, one to regulate the number of muscle fibers that are formed during development and a second to regulate the growth of those fibers postnatally. The sequence of MSTN has been highly conserved through evolution, with the mature MSTN peptide being identical in species as divergent as humans and turkeys (3). The function of MSTN has also been conserved, and targeted or naturally occurring mutations in MSTN have been shown to cause increased muscling in numerous species, including cattle (3–5), sheep (6), dogs (7), rabbits (8), rats (9), swine (10), goats (11), and humans (12). Numerous pharmaceutical and biotechnology companies have developed biologic agents capable of blocking MSTN activity, and these have been tested in clinical trials for a wide range of indications, including Duchenne and facioscapulohumeral muscular dystrophy, inclusion body myositis, muscle atrophy following falls and hip fracture surgery, age-related sarcopenia, Charcot–Marie–Tooth disease, and cachexia due to chronic obstructive pulmonary disease, end-stage kidney disease, and cancer.The finding that certain inhibitors of MSTN signaling can increase muscle mass even in Mstn^−/− mice revealed that the function of MSTN as a negative regulator of muscle mass is partially redundant with at least one other TGF-β family member (13, 14), and subsequent studies have identified activin A as one of these cooperating ligands (15, 16). MSTN and activin A share many key regulatory and signaling components. For example, the activities of both MSTN and activin A can be modulated extracellularly by naturally occurring inhibitory binding proteins, including follistatin (17, 18) and the follistatin-related protein, FSTL-3 or FLRG (19, 20). Moreover, MSTN and activin A also appear to share receptor components. Based on in vitro studies, MSTN is capable of binding initially to the activin type II receptors, ACVR2 and ACVR2B (also called ActRIIA and ActRIIB) (18) followed by engagement of the type I receptors, ALK4 and ALK5 (21). In previous studies, we presented genetic evidence supporting a role for both ACVR2 and ACVR2B in mediating MSTN signaling and regulating muscle mass in vivo. Specifically, we showed that mice expressing a truncated, dominant-negative form of ACVR2B in skeletal muscle (18) or carrying deletion mutations in Acvr2 and/or Acvr2b (13) have significantly increased muscle mass. One limitation of the latter study, however, was that we could not examine the consequence of complete loss of both receptors using the deletion alleles, as double homozygous mutants die early during embryogenesis (22). Moreover, the roles that the two type I receptors, ALK4 and ALK5, play in regulating MSTN and activin A signaling in muscle in vivo have not yet been documented using genetic approaches. Here, we present the results of studies in which we used floxed alleles for each of the type II and type I receptor genes in order to target these receptors alone and in combination in muscle fibers. We show that these receptors are functionally redundant and that signaling through each of these receptors contributes to the overall control of muscle mass.     

余尚贞以六戊年麦门冬汤治疗高血压经验浅析

高血压病为临床最常见的慢性病,余尚贞根据多年临床经验辨证,结合开、阖、枢理论,以太阴阳明升降不和为病机,从太阴阳明入手论治高血压病,结合五运六气选方六戊年麦门冬汤,临床治疗多例,疗效甚佳。开、阖、枢理论源于内经,是对人体三阴三阳经生理功能、病理特点及其相互关系的概括,我们可从中窥得开、阖、枢理论之部分面貌,比如对太阴、阳明经的了解,并拓展中医在治疗高血压病方面的治疗思路。     

补肾壮骨汤对骨质疏松型胸腰椎压缩骨折患者椎体成形术治疗效果影响的Meta分析

[目的]采用Meta分析法系统评价补肾壮骨汤对椎体成形术治疗骨质疏松型胸腰椎压缩骨折(OTCF)临床的影响。[方法]以"补肾壮骨汤"为首输关键词,以"椎体成形术""骨质疏松""胸腰椎压缩骨折"等为次输关键词,全面搜索补肾壮骨汤对OTCF患者椎体成形术治疗效果影响的随机对照研究文献,评价纳入研究文献的一般特征,对文献资料所提取的治疗有效率、骨密度、Oswestry功能障碍(ODI)指数、治疗安全性(新发骨折率)等观察指标进行Meta分析处理与分析。[结果]共13篇文献纳入Meta分析范畴,文献总样本量1 037例。分析显示,与对照组相比,治疗组可明显提高临床有效率[OR=4.63,95%CI[2.92,7.36],P0.000 01]、改善骨密度[MD=0.08,95%CI[0.06,0.1],P0.000 01]、降低ODI指数[MD=-2.34,95%CI[-3.49,-1.19],P0.000 01]、降低新发骨折率[OR=0.08,95%CI[0.11,0.44],P0.000 01]。[结论]与单纯椎体成形术治疗相比,补肾壮骨汤辅助椎体成形术在OTCF患者治疗中,可提升患者术后骨密度、改善胸腰椎功能障碍和降低术后新发骨折率,治疗疗效确切。     

股骨头坏死误诊原因分析

目的:分析股骨头坏死(osteonecrosis of the femoral head,ONFH)的误诊原因。方法:从中国股骨头坏死数据库(China osteonecrosis of the femoral head database,CONFHD)中选择2016年7月至2018年12月就诊,且一般情况、病史、诊疗记录完整的ONFH患者,提取相关信息,统计分析ONFH患者首诊误诊情况及误诊原因。结果:1471例ONFH患者录入的病例资料中一般情况、病史及诊疗记录完整。303例(21%)患者既往误诊,其中被误诊为腰椎间盘突出症118例、髋关节滑膜炎86例、髋关节骨关节炎48例、类风湿关节炎32例、梨状肌综合征11例、坐骨神经痛5例、其他疾病3例。Logistic回归分析结果显示,激素使用史、症状隐匿、首诊医生职称为ONFH误诊的影响因素(OR=1.540,P=0.009;OR=2.195,P=0.000;OR=2.877,P=0.000)。结论:ONFH易被误诊为腰椎间盘突出症、髋关节滑膜炎、髋关节骨关节炎、类风湿关节炎等疾病;患者有激素使用史、症状隐匿、首诊医生为主治医师及以下职称时容易误诊。     

手法复位超腕关节夹板联合石膏托固定治疗Salter-HarrisⅡ型儿童桡骨远端骨骺骨折

目的:探讨手法复位超腕关节夹板联合石膏托固定治疗Salter-HarrisⅡ型儿童桡骨远端骨骺骨折的临床疗效与安全性。方法:2015年11月至2018年11月,收治44例桡骨远端骨骺骨折患者。男35例,女9例。年龄6~17岁,中位数10岁。左侧26例,右侧18例。均为闭合性损伤,根据Salter-Harris分型均属于Ⅱ型,其中不稳定型5例。20例合并尺骨茎突骨折,均不合并神经、血管损伤。均因跌倒致伤,受伤至治疗时间1 h至2 d,中位数8 h。均先进行手法复位,复位后先以超腕关节夹板固定,然后辅以石膏托固定。随访观察骨折愈合及并发症发生情况,测量腕关节活动度,采用Gartland-Werley腕关节评分系统评价综合疗效。结果:43例患者获得随访,随访时间6~24个月,中位数13个月。骨折均愈合,愈合时间(1.5±0.1)个月,塑形时间(3.0±0.5)个月。43例患者腕关节掌屈55°±5°、背伸40°±15°、桡偏25°±5°、尺偏35°±5°,下尺桡关节旋前80°±5°、旋后90°±5°。末次随访时,Gartland-Werley腕关节评分(1.8±0.6)分,优40例、良3例。所有患儿均未发现桡骨远端骨骺早闭。结论:手法复位超腕关节夹板联合石膏托固定可有效治疗Salter-HarrisⅡ型儿童桡骨远端骨骺骨折,安全性高。     

基于高通量测序技术研究药食两用薏苡仁中污染真菌多样性

目的:调查药食两用薏苡仁中污染真菌多样性,为其安全使用提供参考依据。方法:收集薏苡仁样品18批,提取真菌DNA并扩增ITS2序列,基于Illumina MiSeq PE250平台进行高通量测序。结果:共检测到4门18纲44目99科149属的真菌,子囊菌门Ascomycota是最优势菌门,镰刀菌属Fusarium(3.05%~60.32%)是属水平最优势属,其次是曲霉属Aspergillus(2.20%~45.44%)、白僵菌属Beauveria(0.07%~63.21%)、链格孢属Alternaria(0.80%~11.92%)、Arachnomyces(0.03%~39.36%)和青霉属Penicillium(0.24%~8.03%)。此外,共检测到5种潜在产毒真菌,分别是烟曲霉A.fumigatus、土曲霉A.terreus、梨孢镰刀菌F.poae、囊状青霉P.capsulatum和展青霉P.paxilli。结论:高通量测序技术可以快速有效地检测薏苡仁中污染真菌种类,为薏苡仁污染真菌毒素提供风险预警。     

左金丸抗幽门螺杆菌感染的分子网络调控机制研究

目的基于网络药理学和生物信息学方法探究左金丸抗幽门螺杆菌(Hp)感染的分子网络调控机制。方法通过中药系统药理学数据库和分析平台(TCMSP)检索左金丸化学成分,筛选并预测其入血活性成分和作用靶点,检索疾病数据库中与Hp感染相关的作用靶点,构建左金丸成分靶点与疾病靶点的交互网络,获得左金丸抗Hp的特征性基因;通过DAVID6.8数据库对上述特征性基因进行GO功能富集和KEGG通路富集分析;利用Cytohubba筛选出左金丸抗Hp感染的关键靶点。结果通过TCMSP筛选、预测得到左金丸32个入血活性成分和197个作用靶点。GO分析共得到199条富集结果,其中生物过程包含炎症反应、RNA信号转录、信号传导等152条,细胞组分包含细胞核、细胞外基质、蛋白复合物等19条,分子功能包含细胞因子活性、DNA结合、ATP结合等28条。KEGG分析结果显示,Jak-STAT信号通路、T细胞受体信号通路、细胞周期信号通路、Wnt信号通路等65条通路与左金丸抗Hp感染密切相关。经Cytohubba筛选得到CXCL8、IL10、IL4、VEGFA、MMP9等10个关键基因。结论左金丸抗Hp感染具有多成分、多靶点、多通路协同作用的特点,可为其活性成分研究和抗Hp药效及机制研究提供依据。